Story by Emily Padhi, a U of G student writer with SPARK (Students Promoting Awareness of Research Knowledge)
A microscopic component inside every cell in the human body may reveal why exercise can help prevent diabetes.
These components, called mitochondria, are best known as a collection of millions of mini-power plants in the body, generating energy for almost every bodily function imaginable. But Prof. Graham Holloway, Human Health and Nutritional Sciences, thinks mitochondria may also help stave off diabetes.
“When it comes to mitochondria,” he says, “the more the merrier.”
The number of mitochondria in the body can affect your chances of becoming insulin resistant, a condition that can lead to diabetes. Low numbers of mitochondria are associated with an increased risk of becoming insulin resistant, while higher numbers translate to a lowered risk.
Interestingly, it seems exercise can increase the number of mitochondria in the body. At U of G, Holloway and his team are looking at the factors surrounding exercise that promote the creation of more mitochondria.
Here’s what happens. After eating, food is broken down into smaller components: fat into fatty acids, protein into amino acids, and carbohydrates into glucose. As soon as these molecules are detected in the blood, insulin knocks on the door of cells in the liver, fat and muscle so they can “open up” and take in these nutrients.
Fat broken down into fatty acids is either sent to muscle tissue for storage or to the mitochondria, where they are processed to release energy in what is known as fatty acid oxidation. However, if this release of energy is not met with an increase in energy consumption by burning calories, harmful free radicals are generated.
When insulin resistance develops, insulin becomes less effective and cell doors in the liver, fat and muscle stay shut. The result is a reduced ability for fat cells to take in fatty acids, increasing their concentration in the blood.
“Fatty acids tend to generate free radicals, so interventions that promote fatty acid oxidation are likely advantageous in combating the ever-increasing prevalence of Type 2 diabetes,” says Holloway.
Indeed, patients with diabetes are observed to experience higher levels of circulating free radicals, which are thought to be related to a low mitochondria count.
“Ideally, fats undergo oxidation rather than accumulate as fat tissue,” says Holloway, “so it makes sense to find ways to favour oxidation over storage, and one approach is to increase the number of mitochondria found in the tissue.”
Holloway and his team are trying to understand the factors that influence fatty acid oxidation and how promoting this process may prevent insulin resistance from developing. His research is sponsored by the Natural Sciences and Engineering Research Council and the Canada Foundation for Innovation.